Hypertrophic cardiomyopathy (HCM) is infrequently complicated by infective endocarditis (IE). The authors report the case of a 46-year-old woman developing IE in asymptomatic HCM. Blood cultures were positive for Streptococcus viridans. Echocardiography demonstrated: 1) a mobile (1.2 x 1 cm2) vegetation attached to the septal endocardium at the site of contact between the mitral valve leaflet and the hypertrophic septum; 2) two large (2.7 x 1.7 cm2 and 1.6 x 1.1 cm2) vegetations at NCC and RCC respectively of aortic valve, causing moderate valve regurgitation, and, 3) a mural (1 x 0.8 cm2) vegetation on the posterior wall of the left ventricle. On the third day of hospitalization, the patient underwent aortic valve replacement and removal of the vegetations. Antibiotics were continued for another four weeks. The patient recovered and follow-up was uneventful. Thus, chronic endocardial trauma of the septum, a common finding in HCM with outflow tract obstruction, may provide a fertile nidus for the development of vegetation, which in turn would play the major role in the pathogenesis of IE.

Infective endocarditis is a rare complication of hypertrophic cardiomyopathy. It's estimated incidence is 1.4 per 1000 person/year in all patients and it increases to 3.8 per 1000 person/year in patients with left ventricular outflow obstruction. The most common site of vegetation is the ventricular aspect of anterior mitral valve leaflet. We report a case of a 43-year-old man who was admitted for mitral infective endocarditis resulting in severe mitral regurgitation complicating a hypertrophic obstructive cardiomyopathy. The patient underwent mitral valve replacement. Post-operative outcome was good with relieve of symptom and resolution of left ventricular outflow obstruction. Literature data are reviewed.

The most frequent site of vegetative lesion in patients with hypertrophic cardiomyopathy is anterior mitral leaflet, due to chronic endocardial trauma arising from systolic anterior motion. We describe three cases of serious infective endocarditis complicated lesions (vegetation, aneurysm and perforation) on aortic and mitral valves, in patients with obstructive hypertrophic cardiomyopathy. In particular, we observed how severe valvular damage and dysfunction, combined with particular hemodynamic conditions, are followed by adverse clinical outcome. We performed transthoracic echocardiogram and transoesophageal echocardiography studies to define morphologic and hemodynamic features of infection, deciding the proper therapy and we planned the echocardiographic follow-up. Copyright 2002 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved.

BACKGROUND: The literature on infective endocarditis in hypertrophic cardiomyopathy (HCM) is virtually confined to case reports. Consequently, the risk of endocarditis in HCM remains undefined. METHODS AND RESULTS: We assessed the occurrence of endocarditis in 810 HCM patients evaluated between 1970 and 1997. Endocarditis was diagnosed in 10 patients, 2 of whom were excluded from analysis of prevalence and incidence because they were referred for acute endocarditis. At first evaluation, echocardiographic features consistent with prior endocarditis were identified in 3 of 808 patients, a prevalence of 3.7 per 1000 patients (95% CI, 0.8 to 11). Of 681 patients who were followed, 5 developed endocarditis, an incidence of 1.4 per 1000 person-years (95% CI, 0.5 to 3.2); outflow obstruction was present in each of these 5 patients and was associated with the risk of endocarditis (P=0.006). In the 224 obstructive patients, incidence of endocarditis was 3.8 per 1000 person-years (95% CI, 1.6 to 8.9) and probability of endocarditis 4. 3% at 10 years. Left atrial size was also associated with the risk of endocarditis (P=0.007). In patients with both obstruction and atrial dilatation (>/=50 mm), incidence of endocarditis increased to 9.2 per 1000 person-years (95% CI, 2.5 to 23.5). Analysis of all 10 patients with endocarditis identified outflow obstruction in each and atrial dilatation in 7. CONCLUSIONS: Endocarditis in HCM is virtually confined to patients with outflow obstruction and is more common in those with both obstruction and atrial dilatation. These results indicate that antibiotic prophylaxis is required only in patients with obstructive HCM.

The American Heart Association recently revised its guidelines for the prevention of bacterial endocarditis. These guidelines are meant to aid physicians, dentists and other health care providers, but they are not intended to define the standard of care or to serve as a substitute for clinical judgment. In the guidelines, cardiac conditions are stratified into high-, moderate- and negligible-risk categories based on the potential outcome if endocarditis develops. Procedures that may cause bacteremia and for which prophylaxis is recommended are clearly specified. In addition, an algorithm has been developed to more clearly define when prophylaxis is recommended in patients with mitral valve prolapse. For oral and dental procedures, the standard prophylactic regimen is a single dose of oral amoxicillin (2 g in adults and 50 mg per kg in children), but a follow-up dose is no longer recommended. Clindamycin and other alternatives are recommended for use in patients who are allergic to penicillin. For gastrointestinal and genitourinary procedures, the prophylactic regimens have been simplified. The new recommendations are meant to more clearly define when prophylaxis is or is not recommended, to improve compliance, to reduce cost and the incidence of gastrointestinal side effects, and to approach more uniform worldwide recommendations.

A patient with hypertrophic obstructive cardiomyopathy (HOCM) and Staphylococcus aureus mitral valve endocarditis is reported. Bacterial endocarditis occurs with increased frequency and the prognosis is worse in these patients. All patients with HOCM should therefore be given antibiotic treatment every time they undergo invasive procedures to prevent potentially fatal bacteraemia.

Certain clinical and morphologic findings are described in 11 patients with hypertrophic cardiomyopathy complicated by infective endocarditis that produced severe mitral or aortic valve regurgitation, or both, necessitating valve replacement. All 11 patients had changes in the operatively excised valve or valves characteristic of healed infective endocarditis. The infection involved only the mitral valve in seven patients, only the aortic valve in three patients and both valves in one patient. Study of the operatively excised mitral valves indicated that the healed vegetations were located most commonly on the left ventricular aspects of the anterior mitral leaflet, indicating that vegetation had formed at contact points of this leaflet with mural endocardium of the left ventricular outflow tract. In all 11 patients, the infective endocarditis either worsened preexisting valve regurgitation or initiated valve regurgitation and led to worsened signs and symptoms of cardiac dysfunction, necessitating valve replacement. Functional class improved in the nine patients who survived 7 to 101 months after valve replacement. Hypertrophic cardiomyopathy appears to be a factor predisposing to infective endocarditis. Patients with hypertrophic cardiomyopathy should receive prophylactic antibiotic therapy during procedures that predispose to infective endocarditis.

Seven cases of infective endocarditis (IE) in patients with hypertrophic obstructive cardiomyopathy (HOCM) are presented in this report. The previous literature is critically reviewed, and the following points are discussed: (a) IE complicates HOCM in 5-9% of cases; (b) anatomical and haemodynamic alterations of HOCM cause microtraumas on heart valves and the endocardium; the resulting endocardial lesions represent sites for bacterial seeding as well as other congenital or acquired heart disease; (c) prognosis is worse in patients with IE associated with HOCM than in patients with IE alone or associated with congenital heart disease; (d) the most frequently isolated organisms are saprophytes; (e) most patients were exposed to bacteraemias before the onset of IE.

A patient with idiopathic hypertrophic subaortic stenosis suffered from five episodes of infective endocarditis of the mitral valve. At least two of these episodes were caused by Lactobacillus species, a microorganism known to be difficult to eradicate. Definitive cure was only achieved by surgical treatment.

We report a case of bacterial endocarditis due to Actinobacillus actinomycetemcomitans in a man with hypertrophic obstructive cardiomyopathy complicated by a mycotic aneurysm and thrombosis of the right common iliac artery. The patient was successfully treated with a combination of ampicillin and gentamicin, but was left with residual mitral incompetence.

Three cases of infective endocarditis (IE) occurringg in patients with idiopathic hypertrophic subaortic stenosis (IHSS) are described. A review of the literature reveals the IE occurs in about 50 percent of the patients suffering from IHSS. It appears to complicate the natural history of the severe cases, at least as it appears from hemodynamic studies, being precipitated by the same factors and caused by the same infective organisms as in valvular heart disease. It has the same clinical picture and outcome, although the appearance of new murmurs was more common than in other types of heart disease complicated by IE, and indicated the same poor prognosis. The infection seems to involve both the aortic and the mitral valve, with equal frequency, and less commonly the ventricular outflow tract. The need for IE prophylaxis in cases of IHSS is stressed.

In two patients infective endocarditis developed as the primary manifestation of idiopathic hypertrophic subaortic stenosis. Infected vegetations were present on the mitral and aortic valves. In addition, bacterial vegetations were observed on the septal endocardium at the site of contact between the mitral valve leaflet and the hypertrophic septum. Thus, chronic endocardial trauma, a common finding in idiopathic hypertrophic subaortic stenosis, may provide a fertile nidus for the development of bacterial vegetation.

This report describes a patient with hypertrophic obstructive cardiomyopathy complicated by acute aortic and probably mitral valvular incompetence caused by endocarditis due to Staphylococcus aureus. Following the onset of valvular insufficiency, this patient developed hypotension and pulmonary edema and eventually underwent cardiac surgery in an attempt to control these complications. We review the unique pathophysiology of hypertrophic obstructive cardiomyopathy and its alterations in the presence of acute valvular incompetence and analyze the limitations of medical management of cardiac decompensation in patients with this combination of cardiac abnormalities. The possible need for early surgery in such patients is examined.

Three patients with endocarditis caused by Streptococcus mutans were seen during a six-month period. All had clinical features of subacute bacterial endocarditis, including fever, heart murmurs, and positive blood cultures. One had underlying aortic insufficiency and two had idiopathic hypertrophic subaortic stenosis. All patients were treated with parenteral antibiotics and were cured. Streptococcus mutans is a pleomorphic, microaerophilic organism that is associated with dental caries and plaque. Differentiation of S mutans from enterococcal endocarditis is important because the former condition can be treated for a shorter period of time with penicillin alone, without the addition of aminoglycoside antibiotics.

Treatment of idiopathic hypertrophic subaortic stenosis (IHSS) remains a controversial problem and depending upon many factors, medical or surgical treatment may be elected. When medical therapy fails and surgery is recommended, choice of an appropriate surgical technique may be difficult. An analysis is given of 27 patients who have undergone only mitral valve replacement as definitive treatment. Twenty-six patients were dismissed from the hospital with good or excellent results and one died (3.7 percent mortality). Pressure gradients across the left ventricular outflow tract after operation were eliminated in every instance. The mean preoperative gradient was 74 mm Hg and postoperatively was 6.9 mm Hg. Advantages and disadvantages of mitral valve replacement as definitive treatment of IHSS are presented. This method of treatment should be reserved for patients with incapacitating symptoms, congestive heart failure, severe left ventricular hypertension, unusual electrocardiographic findings or in patients who have failed to respond favorably to previous septectomy.

Bacterial endocarditis complicating idiopathic hypertrophic subaortic stenosis (IHSS) is uncommon but endocarditis may be the first clinical manifestation of IHSS. In this report of such a case, the aortic and the mitral valves were the sites of the bacterial infection. Many chordae tendineae to the mitral valve were ruptured from the extension of the infectious process. The endothelial lesions, which served as the seat for the bacterial infection on the anterior mitral leaflet, likely resulted from its abutting action against the septal prominence. Damage to the aortic valve leaflet may have resulted from abnormal valve motion caused by IHSS and created an environment conducive to endocarditis. This patient developed aortic insufficiency during the course of bacterial endocarditis, suggesting that the occasional association of aortic insufficiency in patients with IHSS may be secondary to healed endocarditis of the aortic valve.